Crush Syndrome

Crush syndrome encompasses the systemic manifestations that result from a crush (or traumatic compression) injury. Compartment syndrome and/or rhabdomyolysis can also occur in crush syndrome. Systemic effects include the development of renal failure due to toxins released from damaged muscles, hypovolemia, and acidosis. Other features include arrhythmias from the electrolyte imbalances, ARDS from the inflammatory response, and disseminated intravascular coagulation from liberated thromboplastin. Field management with intravenous fluids and extrication is crucial in reducing the risk of death. Inpatient care requires a multidisciplinary team focused on continued hydration, reducing complications or further injury, and determining the need for operative intervention.

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Definition and Etiology


Crush syndrome is a condition of systemic manifestations (including shock and renal failure) that develop from high-degree crush injury or traumatic compression of the torso, extremities, or other parts of the body.


  • Vehicular accidents (trapped under a vehicle)
  • Industrial, construction, or agricultural accidents
  • Major earthquakes (structure collapse, entrapment > 24 hours is associated with increased mortality)
  • Stampede


Initial events

  • Compression leads to direct tissue damage and venous occlusion.
  • Crush syndrome can also occur with compartment syndrome (when damage is confined within the muscle compartment(s)).
  • Prolonged compression results in rhabdomyolysis.

Systemic effects

  • Renal failure from:
    • Hypovolemia:
      • Enzymes released (including CK) damage capillaries.
      • Leakage of fluid and sequestration in extracellular spaces follow.
      • This process leads to ↓ intravascular volume → renin-angiotensin-aldosterone (RAA) system is stimulated
      • RAA effect: reduced renal blood flow
    • Release of myoglobin from necrotic muscles:
      • Myoglobin is cytotoxic to the nephrons.
      • Myoglobin also results in lipid peroxidation of renal cell membranes.
      • Myoglobin scavenges nitric oxide: ↑ renal injury
      • Other products include free iron, which generates reactive oxygen species (ROS), damaging the renal tubules
    • Metabolic acidosis: ↑ lactic acid from damaged/ischemic muscles
    • Hyperphosphatemia from necrotic muscles:
      • Leads to hypocalcemia
      • Leads to calcium phosphate salts → renal damage
    • Uric acid release: 
      • Nucleosides from cell nuclei → uric acid 
      • Uric acid crystal deposition increases in an acidic environment, leading to tubular obstruction. 
  • Cardiac effect:
    • Reduced intravascular volume → ↓ cardiac output → hypoperfusion of organs
    • Upon extrication, deterioration can lead to immediate death (also called “smiling death”: relief after extrication but cardiac arrest/ventricular fibrillation occurs from hyperkalemia and hypocalcemia).
  • Disseminated intravascular coagulation (DIC): released thromboplastin from necrotic muscles leading to DIC → multi-organ failure
  • ARDS from:
    • Inflammatory response due to multiple injuries
    • Fat embolism (resulting from fractures)
    • Distributive shock
Pathogenesis of crush syndrome-related acute kidney injury

Pathogenesis of crush syndrome-related acute kidney injury:

1) Muscle necrosis leads to intravascular volume depletion, renal hypoperfusion, and ischemia. Acute kidney injury (AKI) is prerenal at the beginning.
2) Myoglobin is liberated from the muscles, and myoglobinuria causes intratubular cast formation (resulting in AKI).
3) Myoglobin scavenges nitric oxide (NO), which aggravates renal hypo-perfusion and tissue injury.
4) Nucleosides (released from disintegrating cell nuclei) produce uric acid, which may contribute to cast formation and tubular obstruction. Release of free iron, which catalyzes free radical production, enhances ischemic damage.
5) Potassium released depresses cardiac output, potentiating renal hypoperfusion.
6) Hyperphosphatemia may contribute to hypocalcemia (causing depressed myocardial contractility) and the precipitation of CaPO4 salts (inducing inflammation of the kidney).
7) Released tissue thromboplastin, triggers disseminated intravascular coagulation.

ARF: acute renal failure
ATN: acute tubular necrosis
DIC: disseminated intravascular coagulation
IVV: intravascular volume
Uric ac: uric acid
Lactic ac: lactic acid
CaPO4: calcium phosphate

Image: “Pathogenesis of crush syndrome” by Sever and Vanholder. License: CC BY 3.0

Clinical Presentation

Chest and abdominal crush injury

  • Chest injury: hemothorax, pneumothorax, pulmonary contusions, rib fractures
  • Chest compression → ↑ intrathoracic pressure → blood from the superior vena cava and right atrium driven into the brachiocephalic and jugular veins
  • Deep inspiration against a closed glottis (Valsalva maneuver) causes back pressure → head and neck capillaries are engorged and eventually rupture:  
    • Subconjunctival hemorrhage
    • Petechial eruptions 
    • Soft tissue edema of the face
    • Craniocervical cyanosis (engorgement causes blood flow stagnation and subsequent desaturation) 
  • Abdominal crush injury: presents with hollow viscus injuries, liver and splenic lacerations
  • Prolonged compression can produce spinal cord injury.
Traumatic asphyxia due to blunt chest trauma

Chest blunt trauma: patient with crush injury with chest CT showing hemopneumothorax and bilateral pulmonary contusions (right more than the left)

Image: “Computed tomography scan” by ICU department, University Hospital of Alexandroupolis, Dragana, Alexandroupolis 68100, Greece. License: CC BY 2.0

Extremity crush injury

  • Extremity crush injury ranges from: 
    • Extremity swelling and erythema
    • Bruising 
    • Open fractures
    • Mangled/deformed extremities
  • Rhabdomyolysis: myalgia, weakness, and dark-colored urine
  • Compartment syndrome: pain, pallor, pulselessness, poikilothermia, paresthesia, and paralysis (the “6 Ps”)
Open fracture of the ankle

Crushing injuries of foot and ankle: Image shows open fracture after initial debridement and fixation.

Image: “Open fracture of the ankle” by D.A. Edelstein and I. Florescu. License: CC BY 2.0

Other clinical features

  • Shock (hypovolemia and/or hemorrhage): hypotension, tachycardia, pallor
  • Acute renal failure: oliguria, anuria
  • Arrhythmia (from acidosis, electrolyte abnormalities):
    • Conduction abnormalities
    • Ventricular tachycardia/fibrillation
    • Asystole
  • Cardiac failure and ARDS: dyspnea
  • DIC: bleeding, petechiae, ecchymoses

Diagnosis and Management

Initial assessment and management

  • Advanced trauma life support (ABCDE):
    • Airway
    • Breathing
    • Circulation
    • Disability: Perform basic neurologic examination.
    • Exposure: Search for injuries, and perform environmental control (prevent hypothermia).
  • Assessment of mechanism of injuries and potential injuries
  • Administration of isotonic saline in the field prior to or as soon as possible after extrication
  • If extrication is not possible due to trapped extremity, field amputation is performed after all options are exhausted.
  • IV hydration and monitoring are continued during transport to the hospital.

Inpatient management

  • Repeat assessment: physical examination including ABCDE assessment
  • Stabilize patient, assess response to initial resuscitation and need for operative intervention.
  • Work-up:
    • Search for potential injuries and perform diagnostic studies:
      • Portable radiographs
      • FAST
      • Emergency CT
      • Electrocardiogram
    • General laboratory studies done on admission and subsequently monitored:
      • Electrolytes, renal function
      • Arterial blood gas
      • Urine myoglobin and CK
      • CBC
      • Coagulation studies
  • Continued IV hydration with urine output monitoring
  • Hemodialysis when indicated
  • Correct electrolyte imbalances (such as hyperkalemia, hypocalcemia).
  • Address metabolic abnormalities (e.g., alkalinization of urine in acidosis).
  • Telemetry monitoring due to risk of arrhythmia
  • Analgesia
  • Injury-specific treatment:
    • Treat open wounds (wound care, antibiotics, tetanus toxoid) and perform debridement when needed.
    • For compartment syndrome, perform fasciotomy. 
    • Management of organ injuries and fractures

Clinical Relevance

  • Acute renal failure: a sudden drop in the glomerular filtration rate from kidney damage that happens within a few hours or a few days. Acute renal failure is classified into prerenal, intrinsic, or postrenal, depending on the etiology. Management is based on causation and often revolves around aggressive fluid hydration. Rhabdomyolysis results in acute tubular necrosis from excessive filtered myoglobin, leading to acute renal failure.
  • Hyperkalemia: a serum potassium (K+) level higher than 5.0 mEq/L. Hyperkalemia is produced by a variety of causes. Acute elevations in serum potassium (usually ≥ 7 mEq/L) can lead to cardiac arrhythmias and muscle weakness. Management involves stabilizing the myocardium, decreasing the extracellular K+ levels, and enhancing K+ removal from the body.
  • Hypocalcemia: defined as a calcium level < 2.2 mmol/L or < 8.5 mg/dL. Calcium levels are regulated by the parathyroid hormone (PTH). If the body fails to maintain normal calcium levels (especially at ≤ 7.5 mg/dL), patients can present with arrhythmias, seizures, and tetany. Management is with calcium replacement.
  • Hyperuricemia: elevated uric acid levels, which can result from accelerated purine degradation (as what occurs in high cell turnover states such as rhabdomyolysis). Large amounts of uric acid deposit in the renal tubules, causing acute renal injury. Management involves aggressive intravenous hydration.
  • ABCDE assessment: the mainstay management approach used in managing critically ill patients and the essential 1st steps to perform in many situations, including unresponsive patients, cardiac arrests, and critical medical or trauma patients. For the trauma patient, ABCDE is included in the primary survey, the initial evaluation, and the management of injuries. 
  • Rhabdomyolysis: a condition characterized by muscle necrosis and the release of myoglobin, which is nephrotoxic. Rhabdomyolysis can be traumatic (by direct muscle compression) or nontraumatic (e.g., intense exertional activity). Creatine kinase elevation with presentation of myalgias and dark urine highly suggest the diagnosis. Management is with IV fluid resuscitation. 
  • Compartment syndrome: a surgical emergency occurring secondary to trauma. The syndrome is marked by increased pressure within a compartment that compromises the circulation and function of the tissues. Long bone fractures are the most common cause. Patients can present with pain, pallor, pulselessness, paresthesia, poikilothermia, and paralysis (the 6 Ps). Diagnosis is clinical but compartment pressure measurement can be used. Management is an emergency fasciotomy.


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